Functionally impaired, hypertrophic ECL cells accumulate vacuoles and lipofuscin bodies - An ultrastructural study of ECL cells isolated from hypergastrinemic rats

Citation
Cm. Zhao et al., Functionally impaired, hypertrophic ECL cells accumulate vacuoles and lipofuscin bodies - An ultrastructural study of ECL cells isolated from hypergastrinemic rats, CELL TIS RE, 303(3), 2001, pp. 415-422
Citations number
25
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL AND TISSUE RESEARCH
ISSN journal
0302-766X → ACNP
Volume
303
Issue
3
Year of publication
2001
Pages
415 - 422
Database
ISI
SICI code
0302-766X(200103)303:3<415:FIHECA>2.0.ZU;2-R
Abstract
ECL cells in the oxyntic mucosa of stomach control gastric acid secretion b y mobilizing histamine in response to gastrin. They respond to gastrin also with hypertrophy and hyperplasia. ECL cells exhibit functional impairment upon long-term gastrin stimulation. The impairment is manifested in a gradu al decline of the activity of the histamine-forming enzyme per individual E CL cell and in a failure of gastrin to mobilize histamine. The mechanism be hind this impairment is unknown. In the present study. rats were treated wi th the proton pump inhibitor pantoprazole for 45 days to induce sustained h ypergastrinemia. The ECL cells were isolated from normogastrinemic and hype rgastrinemic rats and size-separated from other mucosal cells by the elutri ation technique. The total ECL cell number was twofold higher in hypergastr inemic rats than in normogastrinemic rats, and most of the cells appeared i n elutriation fractions where large cells predominate. The ECL cells of the different fractions were analyzed by quantitative electron microscopy. Nor mal-sized ECL cells from hypergastrinemic rats displayed a reduced number o f secretory vesicles (probably because of degranulation) compared with norm al-sized ECL cells from normogastrinemic rats. Hypertrophic ECL cells from hypergastrinemic rats had an unchanged number of secretory vesicles, suppor ting the view that such cells fail to respond to gastrin with degranulation . Although both normal-sized and hypertrophic ECL cells from hypergastrinem ic rats contained vacuoles, those in the hypertrophic ECL cells were larger and more numerous. In addition, hypertrophic ECL cells were found to conta in numerous, prominent lipofuscin bodies which are the presumed end product of crinophagia. Conceivably therefore, large vacuoles and lipofuscin bodie s cause functional impairment of the hypertrophic ECL cells.